Effective management of acute stroke patients has remained elusive to the present date. Recent evidence indicates that increased cytokine levels and leukocyte and endothelial cell activation may play a major role in secondary neuronal injury after acute focal cerebral ischemia. The purpose of this investigation is to more clearly characterize the role of the inflammatory response after ischemic injury in humans with regard to its causal influence on secondary neuronal injury and predictive value for long-term functional outcome. Blood samples are drawn from acute stroke patients on admission and serially for the first 7 days. Serial neurologic exams are being performed and MRI scan of the head is done within the first 3 days of admission to determine infarct size. Depression scales are done within the first 14 days. All patients are being seen at 90 days after the ischemic event for follow up at which time blood cytokine levels, neurologic outcome scales, and depression scales are being performed. Through analysis of the advent and duration of cytokine activation, we hope to establish a correlative relationship between the postischemic inflammatory response and neuronal injury. Given the published work demonstrating neuronal protection after ischemia in animal models with antagonists of leukocyte activation and of the inflammatory pathways, we expect these results to establish a temporal window for future drug trials in reducing infarct size after acute stroke. In addition, since clinical outcome in stroke is also dependent on rehabilitation effort, the incidence of depression in stroke patients becomes an important variable in long-term outcome. Thus, we will observe the incidence of depression in stroke patients as it relates to the volume and location of cerebral infarction. A novel approach of correlating sleep architecture in stroke patients with the incidence of mood disturbance will be performed by obtaining a polysomnogram in patients 3-6 months after the ischemic event. A comparison will be made between patients with and without depression. Polysomnograms will also be compared against those of patients with primary depression (who display a very characteristic sleep pattern). It is hypothesized that the mood disturbance in stroke patients may actually be a result of altered sleep patterns caused by the neuronal injury. This may lead to a new understanding of the etiology of mood disorders in stroke patients and aid in their treatment.